Identification of ARKL1 as a Negative Regulator of Epstein-Barr Virus Reactivation

Author:

Siddiqi Umama Z.1,Vaidya Anup S.1,Li Xinliu1,Marcon Edyta2,Tsao Sai Wah3,Greenblatt Jack12,Frappier Lori1ORCID

Affiliation:

1. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada

2. Donnelly Centre, University of Toronto, Toronto, Ontario, Canada

3. School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China

Abstract

Epstein-Barr virus (EBV) maintains a life-long infection due to the ability to alternate between latent and lytic modes of replication and is associated with several types of cancer. We have identified a cellular protein (ARKL1) that acts to repress the reactivation of EBV from the latent to the lytic cycle. We show that ARKL1 acts to repress transcription of the EBV lytic switch protein by inhibiting the activity of the cellular transcription factor c-Jun. This not only provides a new mechanism of regulating EBV reactivation but also identifies a novel cellular function of ARKL1 as an inhibitor of Jun-mediated transcription.

Funder

Gouvernement du Canada | Canadian Institutes of Health Research

Research Grants Council, University Grants Committee

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

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